Short photoperiod, prolonged cold exposure, lactation and food deprivation all produce anovulation in the female hamster. The neuroendocrine changes associated with these four anovulatory syndromes are generally similar and the ovarian consequences appear histologically identical. It appears that multiple stimulus pathways converge on hypothalamic-pituitary mechanisms to block ovulation via common neuroendocrine mechanisms. The present proposal seeks to describe these mechanisms in hamsters in which ovulation is blocked by food deprivation at a specific phase of the reproductive cycle. The neuroendocrine changes in this preparation are subject to better experimental control than they are in the other anovulatory syndromes. Futhermore, the phasic deprivation paradigm may serve as a model system for the study of the dynamic neuroendocrinology of anorexia nervosa. Phasically food deprived, anovulation and normal hamsters will be used to: 1. describe the changes in estradiol, progesterone, cortisol, corticosterone, LH, FSH prolactin, and hypothalamic LHRH during the estrous cycle; 2. examine the role(s) of estradiol and progesterone in the regulation of the ovulatory gonadotropin surge and hypothalamic responsiveness to LHRH; 3. investigate the effectiveness of gonadotropin therapy for the reinstatment of ovulation. In accomplishing these goals, radioimmunoassays for the hormones and constant or pulsatile infusion methods for delivering the gonadotropins will be employed.